A 36-year-old lady underwent revisional bariatric surgery 18 months earlier for weight regain, and after a protracted course in hospital, ultimately died as a result of fulminant hepatic failure.
She had initially undergone a laparoscopic gastric band several years earlier, but due to complications of slippage, she had a subsequent removal. She then underwent a second stage conversion to a roux-en-y gastric bypass a few months later.
During the subsequent 18 months, she suffered chronic intestinal complaints including loose bowel movements, and in the few months leading up to her death, developed worsening hepatic function.
Specialist hepatology and liver transplant input was sought, and it was theorised that intestinal failure was a key contributing factor to her hepatic failure. For this reason, corrective surgery was considered including reversal of bypass, but given her severe malnutrition, a feeding gastrostomy via the remnant stomach was performed instead in attempt to correct any intestinal failure as a contributory factor. However, despite maximal enteral feeding, her hepatic failure worsened in enzymatic and synthetic function.
All investigations for alternative causes were negative, including serum ceruloplasmin, alpha-1-antitrypsin, viral serology, porphyria and autoimmune screens. A liver biopsy demonstrated severe hepatic steatosis with steatohepatitis, likely alcohol related. HIDA scan revealed no biliary excretion, which raised concerns for a non-functioning liver.
During her hospitalisation, collateral history was obtained from her family, which revealed a significantly higher alcohol intake than that which was originally declared. It was determined that the patient consumed roughly 7-10 standard drinks per evening.
Consultation with a liver transplant team was arranged, but sadly at this stage she had developed multi-organ failure secondary to severe sepsis, resulting in cardiovascular collapse refractory to vasoactive therapy, respiratory failure despite maximal ventilatory supports and renal failure with dialysis dependency, and as a result was deemed not surgically fit for transplant. The patient subsequently died despite maximal medical therapy and supportive cares.
A post-mortem was not performed at the request of the patient’s family, however it is theorised that her liver failure was likely caused by a combination of metabolic changes post bypass and the previously undeclared severe alcohol misuse.
Liver failure post bariatric surgery is an extremely rare but documented severe complication. The mechanisms by which this occurs is not entirely clear, but there are indeed case reports in the literature . It is mostly associated with the more malabsorptive procedures such as biliopancreatic diversion and roux-en-y gastric bypass. Literature review suggests that the underlying hepatic insult culminates interestingly in that of severe steatohepatitis, which is consistent with our case.
Paradoxical persistence of steatohepatitis post metabolic surgery appears to be a common entity amongst the case reports in the literature. The underlying aetiology is still unclear, but to date it appears that it may be a complex interplay of humoral responses, cytokine reactions and a severe inflammatory state. In addition to this there have been reports of small intestinal bacterial overgrowth resulting in malabsorption and transit issues as potential contributing factors, suggesting a microbiological aetiology.
Of note, the literature suggests that revisional bariatric surgery in itself is not a predictive factor.
In our case, it seems alcohol was an underappreciated contributing factor. Aside from alcohol, there were no other predictive risk factors in the patient’s profile that would have predisposed her to develop liver failure. To this end, it would seem appropriate to consider such severe alcohol intake a relative contraindication to bariatric surgery without appropriate preoperative optimisation and rehabilitation.